Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A plasma free protein S deficiency was detected in 41 of 63 patients infected with the human immunodeficiency virus type I (HIV-1). This study consisted in a prospective analysis of blood samples from 26 patients with confirmed diagnosis of AIDS, two with AIDS-related complex, 10 with polyadenopathy, and 25 who were asymptomatic. Protein S levels were compared to a matched control group of 24 healthy subjects. A deep venous thrombosis occurred in three AIDS patients with free protein S deficiency. A significant decrease in plasma free protein S levels was observed in HIV-1-seropositive patients (mean +/- SD, 56.5 +/- 23.3%) as compared with control subjects (105.3 +/- 18%, p = 0.0001). Free protein S levels were significantly lower in patients with full-blown AIDS (37.6 +/- 12.3%) than in patients without AIDS (69.8 +/- 19.9%, p = 0.0001). Low plasma free protein S levels correlated with high beta 2-microglobulin values (p = 0.0001), low CD4+ T-cell counts (p = 0.0002) and elevated urinary neopterin concentrations (p = 0.005). According to a multiple regression analysis, the progression to stages IVB, IVC1 or IVD of the Centers for Disease Control (CDC) appeared to be the main explanatory variable in free protein S-deficient patients. Such results suggest that free protein S deficiency may coincide with the development of AIDS. This could contribute to hypercoagulability and, in some instances, thromboembolic complications in AIDS patients.
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PMID:Acquired protein S deficiency: correlation with advanced disease in HIV-1-infected patients. 841 70

A case of warfarin-induced dermatitis in a 79 year-old patient with Protein S deficiency is described. Both total Protein S antigen and free Protein S were moderately reduced (about 50%). The skin lesion did not progress to frank necrosis and it was associated with elevated creatin phosphokinase (CPK) levels in plasma and with thrombosis of the anterior tibial vein localized to the area of dermatitis (probably warfarin-induced deep venous thrombosis). After warfarin withdrawal and beginning of heparin therapy, serum CPK rapidly normalized and the skin lesion improved.
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PMID:Warfarin induced dermatitis and venous thrombosis in a patient with Protein S deficiency. 183 Jun 3

Inherited deficiencies of protein S, an inhibitor of the coagulation system, are now recognized as occurring at least twice as frequently as antithrombin III deficiency in patients with venous thrombosis. Protein S is present in plasma in a complexed form, which is inactive, and in a free or functional form. Free protein S combines with activated protein C to inhibit factors V and VIII. This report describes the evaluation of a family with recurrent deep venous thrombosis and superficial thrombophlebitis. Levels of antithrombin III and protein C as well as plasminogen were normal. The levels of total protein S, which includes the value for the free and complexed forms of protein S, were also normal. However, the free protein S levels were greatly reduced in all symptomatic members who were studied. This report illustrates the importance of obtaining measurement of free protein S levels in patients who are suspected of having inherited venous thrombotic disorders.
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PMID:Free protein S deficiency in a family with venous thrombosis. 214 6

The authors observed a patient with severe inflammatory bowel disease (IBD) complicated by ten episodes of deep venous thrombosis (DVT). Her unusual thrombotic tendency prompted further investigation for primary hypercoagulability. A nonfamilial deficiency of Protein S was documented suggesting the deficiency was acquired. This occurrence suggests that low Protein S levels should be considered as a potential etiologic factor in patients with IBD and recurrent DVT.
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PMID:Deep venous thrombosis, inflammatory bowel disease, and protein S deficiency. 297 96

The fibrinolytic system was investigated in 120 patients with spontaneous or recurrent deep vein thrombosis (DVT) without any known organic disease able to explain by itself the occurrence of a thrombosis and without any known defect of antithrombin III, Heparin Cofactor II, Protein C, or Protein S. The assays included: Euglobulin fibrinolytic activity (EFA), tissue-type plasminogen activator related antigen (t-PA-Ag) and plasminogen activator inhibitor activity (PA inhibitor), which were measured before and after 10 min of venous occlusion (V.O.). On the basis of the results, the patients could be classified in 3 groups: good responders with an at least two-fold increase of EFA after venous occlusion (n = 76), poor responders with a lesser increase of EFA due to deficient release of t-PA (n = 12), and poor responders with a normal t-PA release but an increased level of PA-Inhibitor (n = 32). The poor responders due to deficient t-PA release (10% of total) had a higher incidence of recurrence of deep vein thrombosis, than the other groups (p less than 0.01). An overall correlation was found between the level of PA-Inhibitor activity and the triglyceride level (r = 0.40, p less than 0.01), suggesting that these elevations may be due to a common cause, at least in some of the patients. It is concluded that a poor fibrinolytic response to venous occlusion occurs in 35 percent of DVT patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Deficient t-PA release and elevated PA inhibitor levels in patients with spontaneous or recurrent deep venous thrombosis. 310 59

One hundred and thirty unrelated patients with recurrent deep venous thrombosis were studied over a period of 4 years (1986-1990) in order to determine the possible etiology. Protein C levels were estimated in plasma both by chromogenic substrate assay and by immunoassay. Protein S levels in plasma was determined by immunoassay using antisera to human protein S. Antithrombin III (AT-III) was assayed using monospecific rabbit antiserum to human AT-III. Fifteen patients were found to have hereditary protein C deficiency (11.52%). Family studies revealed autosomal recessive inheritance in one patient and a dominant pattern in the remaining 14 patients. Protein S deficiency was found in eight cases (6.1%), AT-III deficiency was established in five cases (3.8%) and a fibrinolytic defect in 33 cases (25.4%). Thrombosis of visceral and cerebral vessels and a positive family history were more frequently found among patients who had hereditary deficiency of one or the other antithrombotic factor. Thrombophlebitis of superficial veins was found to be very common in patients with protein C and protein S deficiency and virtually absent in AT-III deficiency. The high frequency of protein C and protein S deficiency in this ethnic group is attributed to the high frequency of consanguinity.
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PMID:Thrombophilia in ethnic Arabs in Kuwait. 900 58

Nephrotic syndrome is a hypercoagulable state with variable prevalence of clinical thrombosis. The role of platelet aggregation, fibrinogen and antithrombin III and protein S levels in the pathogenesis of hypercoagulable state in these patients is controversial. Since no study on Indians is available, the clinical and laboratory profile of 22 patients of nephrotic syndrome (age 18-35 years with an MF ratio of 4:3), have been studied. The coagulation profile revealed a prolonged APTT in 12 patients (54.5%), and a prolonged TT in four (18.1%). In the rest APTT and TT were normal. PT was raised in two patients. Fibrinogen, an acute phase reactant was raised in five patients (22.7%). Antithrombin III levels were reduced in 19 patients (86.4%), normal in one and raised in two patients. Free Protein S levels were high in 12(54.5%), normal in seven and decreased in three patients. Platelet aggregation with adrenaline and adenosine diphosphate was raised in 6 patients. Ultrasonographically detected deep vein thrombosis was seen in one patient only (4.5%) who had ATIII levels of 48%. This low incidence can be explained by elevated protein S levels which was found to be raised in 12(54.5%) cases, protein S being an anticoagulant factor. This low level of clinical thrombosis in Indian patients of nephrotic syndrome may be an ethnic variable factor. It is thus concluded that although patients with nephrotic syndrome have a hypercoagulable state, clinical thrombosis is rarely seen in Indian patients with nephrotic syndrome.
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PMID:Prothrombotic factors in nephrotic syndrome. 1121 79

Infection with human immunodeficiency virus (HIV) may lead to hemostatic imbalances. Forty-nine consecutive patients with acute opportunistic infections were screened for thrombophilic parameters. A follow-up investigation was performed after 10 +/- 8 weeks in 26 patients. In acutely ill patients, the incidence of protein S deficiency was 67% (33/49) and of protein C deficiency 25% (12/49), while at the follow-up visit the incidences were 54% (14/26) and 8% (2/26), respectively. Protein S and protein C levels increased significantly from initial to follow-up visit (p < 0.05). Lupus anticoagulants were not detected and anticardiolipin IgG antibodies were present in 11.4% (5/44). Three patients presented with deep venous thrombosis on admission; in two, protein S or protein C deficiency was observed. In conclusion, an acquired protein S and protein C deficiency often develop in patients with HIV and acute illness; this may be reversible after treatment for opportunistic infections.
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PMID:Acquired protein C and protein S deficiency in HIV-infected patients. 1465 42

The Protein S Italian Team (PROSIT) enrolled 79 protein S (PS) deficient families and found 38 PROS1 variations (19 novel) in 53 probands. Of these, 23 variants were selected for expression in'vitro, to evaluate their role as possible causative variants. Transient expression showed high secretion levels (>75%) for three variants, which were considered neutral. Seven missense and five nonsense variants showed low (<or=11%) expression levels and were classified as severe defects. Intermediate expression was observed for eight variants, which were evaluated by factor Va inactivation assay in order to be globally classified as severe or intermediate. Based on the cumulative data, the hazard ratio associated with causative variants was 4.9 (95% CI: 1.4-17.7) for deep vein thrombosis and/or pulmonary embolism, 5.1 (95% CI: 1.1-23.9) for superficial thrombophlebitis, and 4.8 (95% CI: 1.8-13.0) for any venous thrombosis. The hazard ratio for deep vein thrombosis and/or pulmonary embolism in carriers of severe defects only was 7.4 (95% CI: 1.6-24.1). PROSIT showed that dysfunctional variants causing PS deficiency are more common than expected and confirmed that PS deficiency is associated with increased thrombotic risk, although risk assessment is complicated by molecular heterogeneity.
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PMID:Molecular diversity and thrombotic risk in protein S deficiency: the PROSIT study. 1571 27

Protein S is a natural anticoagulant. Congenital protein S (PS) deficiency is a confirmed risk factor of venous thromboembolism (DVT) which though occurs infrequently yet is a leading cause of maternal mortality and morbidity. Congenital PS deficiency may also be responsible for obstetric complications such as preeclampsia/eclampsia, recurrent fetal loss and intrauterine fetal restriction. Congenital PS deficiency has been identified in 1-7.5% of patients with DVT and in 0.03-0.13% general Caucasian population. However, Japanese people have higher prevalence both in VTE patients (12.7%) and general population (0.48-0.63%). Because PS deficiency is the most frequent congenital thrombophilia in Japanese people, Japanese obstetricians must understand this thrombophilia and also that women with PS deficiency have an increased risk of VTE and a necessity of prophylactic use of anticoagulant against recurrent VTE during pregnancy and puerperium. This article reviews the literature to understand PS and congenital PS deficiency, especially the association of this thrombophilia with pregnancy.
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PMID:Protein S and congenital protein S deficiency: the most frequent congenital thrombophilia in Japanese. 1602 79


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